Cs and Theca cells (TCs) of ovarian follicles and regulated the levels of cAMP and steroid production by means of activation of ADRB2/cAMP/protein kinase A (PKA) signaling pathway and/or ADRB2/ cAMP/protein, phospholipase C (PLC)/protein kinase C (PKC)/cAMP response element-binding protein (CREB) signaling cascade [402]. Nevertheless, the excessive ovarian RIPK1 supplier steroidal response to STAT3 web gonadotropins and beta-adrenergic stimulation enhanced polycystic ovary syndrome (PCOS), an endocrine disorder characterizedSun et al. BMC Genomics(2021) 22:Web page 9 ofFig. 4 Scatter plot of annotated differently expressed genes and enriched signaling pathways in LYF follicles among JB and LB chickens. A MA plot of differently expressed genes in GWF follicles involving JB and LB samples. JB3, LYF follicle samples of JB hens; LB3, LYF samples of LB hens. B Bubble chart of top 20 of KEGG pathway enrichmentby anovulation, hyperandrogenism and polycystic ovaries [36, 37, 43, 44]. The a lot abundant expression levels of ADRB2 gene might induce layer broodiness by activation of adenylate cyclase by way of the action of G proteins and stimulate anovulation [37, 43]. The hydroxysteroid (17beta) dehydrogenase type 1 (HSD17B1) can be a steroidogenic enzyme encoded by HSD17B1 gene, to effectively catalyze reversible interconversion of a low-active precursor estrogen estrone (E1) to the extremely active E2 that is certainly necessary for typical ovary development [13, 45]. It truly is the important isozyme within the granulosa cells of your ovary and has a central role in regulating the circulating estradiol concentration also as its local production in estrogen target cells, locally promotes development, differentiation, and maturation from the follicle [468]. Nevertheless, inhibition of HSD17B1 impairs the synthesis of 17-estradiol, and attenuates action in the estradiol [47, 49], which can directly block ovarian follicle improvement. Additionally, HSD17B1 plays a essential function in controlling cell proliferation and within the regulation on the growth and function of organs [50]. It was recommended that the reduced expression levels of HSD17B1 transcript in SYF follicles of JB hens may possibly affect ovarian dominant follicle selection and follicle development and function by repressing 17-estradiol production and follicle cell proliferation, and ultimately bring about a low egg production. Transcriptomic analysis of LYF follicles revealed higher mRNA levels of CYP2D6, CRH, GABRA1, and GHRHRLR, and lower mRNA levels of ID4, SSTR2, CDKN1Aand NDUFAB1 genes in the JB than in the LB layers. Amongst them, the most representative gene GHRHRLR, also named VIPR1, its encoding product VIPR1 was primarily expressed in granulosa cells and residual ovarian tissue [51]. PACAP may promote oocyte maturation within the maturation phase via VPAC1-R on the follicle cells, whose expression surges in full-grown follicles prior to maturation and is regularly high within the follicles undergoing final maturation [35]. In addition, the genetic polymorphisms of VIP and VIPR1 genes were associated with chicken broodiness and egg production [52, 53]. It was intimated that the greater expression levels of VIPR1 transcript in LYF follicles of JB hens might inhibit ovarian follicle growth, differentiation and maturation, and contribute towards the reduced egg production. Interestingly, the significantly up-regulated GABRA1 mRNA and down-regulated NDUFAB1 mRNA from the GWF, SYF and LYF follicles have been co-expressed differentially in JB hen ovaries when compared with LB hen. Preceding studies have reported t